ABSTRACT
Atherosclerosis is a multifactorial disease with a complex pathogenesis. Multiple factors were shown to be involved in atherosclerotic lesion formation, and many knowledge gaps still remain. Mitochondrial dysfunction affects the cellular energy balance, metabolism and survival, and results in the development of mitochondrial cytopathies. These diseases can be caused both by nuclear genes encoding mitochondrial proteins or by mtDNA mutations that affect either mitochondrial proteins or transport RNA (tRNA). In this chapter, the authors summarize the current knowledge on mtDNA mutations and mitochondrial dysfunction as pathophysiological factors of atherosclerosis development. Accumulating evidence indicates that mtDNA mutations play a role in atherosclerosis development alongside with nuclear genome polymorphisms. An important part of mitochondrial proteins that are indispensable for proper functioning of the respiratory chain and energy production are encoded by mtDNA. The acquired knowledge on the mitochondrial involvement in the development of atherosclerosis and chronic inflammation will be used for designing more selective, mitochondria-targeting treatments.
